Infantile autism is a behaviorally defined syndrome first described by Kanner in 1943 (1). The onset prior to 30 months of age. It is characterized by a pervasive lack of responsiveness to people, delayed and deviant language development, and bizarre responses to the environment (such as repetitive or ritualistic behavior) (2). Early suggestions about the etiology of autism centered around psychogenic factors (e.g., emotionally cold mothers). Recent evidence, however, implicates neurobiological factors, an important expression of which is cognitive dysfunction. Since cognition is a dynamic processing of information involving moment-to-moment neuronal changes in responses to events in the environment, and since there are no animal models of autism, an appropriate neurobiological approach to this cognitive dysfunction should reflect such processing in the child with autism. One such neurobiological approach is to investigate the long-latency cognitive components of the event-related brain potential (ERP). Clinical and research evidence suggests that cognitive dysfunction in autism includes defective mechanisms involving alerting to novel information, stimulus categorization, and extraction of meaning from a context. Several components of the ERP have been shown to reflect each of these processes (i.e., alerting to novelty, etc.) in normal children and adults. We propose to show (a) how cognitive ERP components in children with autism differ from those in normal children and (b) that in children with autism, the extent of behavioral impairment is correlated with the extent to which their ERP components differ from normal. This information will be important in refining models of the neurobiology of autism and will, thereby, contribute to efforts at improving methods for establishing diagnoses, prognoses, appropriate educational programs, and rehabilitation assessments for children with autism.